1. Technical Field of the Invention
This invention pertains generally to the field of electrical heart pacemakers, including atrial and ventricular heart pacemakers, and more specifically to a method and apparatus for attenuating polarization voltages at the heart tissue-electrode surface interface following the delivery of a pacing stimulus to the heart tissue.
2. Description of the Prior Art
Heart pacemakers are designed for use on patients whose heart exhibits a failure in the conduction system which manifests itself in many ways, including slow or non-existent heart rates or disassociation of the synchronous contraction of the atrium and the ventricle of the heart. For example, atrial synchronous pacemakers are designed for use on patients whose hearts have normal atrial self-pacing but, due to a defect in the conduction from the atrium to the ventricle, the ventricles fail to beat or keep pace with the atrial depolarization. Irrespective of whichever pacemaker system is actually employed to restore the rhythm of the heart, all operate in a fashion to stimulate excitable heart tissue cells adjacent to the electrode of the pacing lead employed with the pacemaker.
Each heart cell contains positive and negative charges due to the selective absorption of certain ions, such as potassium and sodium through the cell membrane. When the cell is at rest, the inside of the cell is negatively charged with respect to the outside. A stimulus of any kind applied to the cell membrane causes the permeability of the cell membrane to change and allows the ingress of positive charge ions. The resulting dissipation of the negative charges constitutes the "depolarization" of the cell. Simultaneously, the cell contracts causing (in conjunction with the contraction of adjoining cells) the heart muscle to contract. Thus, the stimulation of the heart muscle affects both the contraction of the heart and the depolarization of the once-polarized myocardial cells which make up the muscle.
Following depolarization and contraction of a heart cell, the "repolarization" or recovery of the cell, so that it is ready to receive the next stimulus, commences. During the repolarization time interval, the cell membrane begins to pump out the positive-charged ions that have entered following the application of the stimulus, that is, during the depolarization of the cell. As these positive charges leave, the inside of the cell membrane starts to become negative again and the cell relaxes. In this state, a potential difference builds up, and the cell is said to be repolarized.
The individual myocardial cells are arranged to form muscle sheets which, in gross, constitute the heart itself. The depolarization and repolarization signals of the ventricle, viewed by an electrocardiogram (ECG) are referred to as the QRS wave and the T wave, respectively. The sequence of depolarization that manifests itself in a contraction of the heart muscle and repolarization which manifests itself in the relaxation and filling of the interior chambers of the heart with blood is accomplished through a system of specialized muscle tissue that functions like a nerve network. This system provides electrical stimulating pulses, at a rate which is appropriate for the body's needs. The system then conducts these impulses rapidly to all the muscle fibers of the ventricles, ensuring coordinated, synchronized pumping. It is when this system fails, or is overriden by abnormal mechanisms, that an electronic pacemaker may be needed to generate the triggering stimulus and maintain proper heart rate and synchronization of the filling and contraction of the atrial and ventricular chambers of the heart.
A further phenomena, "polarization voltage" manifests itself at the electrode-tissue interface upon the delivery of a pacemaker stimulation pulse to the tissue.
The polarization voltage is an electrochemical potential, represented by the accumulation of a layer of opposite charges at the electrode-tissue phase boundary during the stimulation pulse. Polarization voltage rises to a peak during the stimulus pulse and then decays by defusion into the tissues, usually disappearing within 100 to 500 msec, before the subsequent pacemaker pulse. Polarization effect is inversely realted to the electrode surface area and directly related to the pulse width.
A pacemaker of relatively short refractory period may sense a prolonged voltage decay waveform or pulse after potential and induce recycling from its own stimulus discharge. The emergence of a prolonged escape interval that is recycled by the pacemaker polarization effect and includes one refractory period and one automatic interval is designated "double reset." A constant regular prolongation of the escape interval that includes the pacemaker automatic interval and its refractory period can be related to sensing of an inapparent signal that occurs immediately outside the refractory period of the pacemaker; this ECG finding should arouse suspicion of oversensing secondary to T wave voltage and/or pacemaker polarization voltage.
This description of the polarization voltage appears in the textbook Cardiac Pacing--A Concise Guide to Clinical Practice, Phillip Verriale, M.D. and Emil Naclerio, M.D., published in 1979 by Lee and Febiger, page 299.
These authors further state that the oversensing may be due to P wave sensing at the ventricular lead, if the lead is poorly positioned. In any case, in a classic single-chamber pacemaker, oversensing may be caused by the effects of the residual polarization voltage and/or the T wave and/or the P wave occuring at the end of the sense amplifier refractory interval. These authors conclude that "Oversensing due to pacemaker polarization effect, although rare, may continue to be a problem with pulse generators that offer a relatively short refractory period and longer stimulus pulse width of 1.5 msec or more, when used with an electrode of small surface area." (page 299).
This background information is useful in understanding the nature of the problem which had led to the method and apparatus of the present invention. The operation of a heart muscle itself, that is the polarization of the cell membrane, the depolarization in response to a stimulus and the subsequent repolarization suggests that the electrode-tissue interface operates in a fashion similar to a capacitive reactance. In reference to FIG. 1, the electrode-tissue interface can be represented through an electrical impedance which constitutes a series resistor R.sub.S in series electrically with the parallel combination of a Faraday resistor R.sub.F and a Helmholtz capacitor C.sub.H. The resistor R.sub.S has a nominal value of about 10-200 ohms, the capacitor C.sub.H has a nominal value of about 5-50 microfarads, and the resistor R.sub.F has a nominal value of 2-100 kilo ohms. These values apply for the impedance measured in gross terms across the output terminals of the pulse generator. In the latter case the value of series resistor R.sub.S may reflect the lead and tissue resistance (about 100 ohms typically). These values vary with pacing stimuli.
In the field of cardiac pacing, the depolarization and repolarization phenomena has affected the ability of the pacemaker sense amplifier to respond accurately and reliably to signals at its input terminal (which is typically connected to the output terminal of the pulse generator) during the repolarization time interval. Pacemaker sense amplifiers are commonly designed to respond to slew rates of the signal at the input terminals, and the repolarization voltage superimposed on the polarization voltage may present a high enough slew rate to create a false triggering problem known as T wave sensing. Certainly the slew rate of the polarization voltage waveform A, FIG. 2, presents a serious problem for a sensitive sense amplifier. In the past, typical pacemaker sense amplifier design has involved the employment of a relatively long refractory interval following the delivery of the stimulation pulse to correspond generally to the heart's own refractory interval, that is, the interval during which the myocardial cells will not react to reapplication of a further stimulus. This has meant that the sense amplifier output signals during the refractory interval have either been ignored or suppressed in past sense amplifier design. The prior art sense amplifier is, therefore, only made responsive to signals at the input terminals manifested after the lapse of the refractory period and the repolarization interval.
The more recent developments of atrial and ventricular pacemakers has made it desirable to be able, at the ventricular sense amplifier for example, to sense the presence or absence of a ventricular depolarization following an atrial stimulus. In addition, it has been considered desirable to be able to verify the capture of the heart by a pacing stimulus by sensing for an evoked depolarization shortly following the delivery of a pacing stimulus. The slew rate of the polarization voltage has in these instances complicated the design of such circuits.
A further complication to pacemaker sense amplifier design lies in the charge and recharge cycle of the pacemaker output capacitor. Typically, the stimulus delivered to the heart is generated by discharging an output capacitor coupled in the output terminals of the pulse generator which, in turn, are adapted to be coupled through a pacing lead to pacing electrodes and to the heart impedance depicted in FIG. 1. The discharge of the pacing capacitance into the capacitive reactance of the heart results in a complex voltage discharge curve at the input terminals of the sense amplifier (which is typically rendered inoperative during the discharge interval of the output capacitor). The recharge of the output capacitor takes place at the end of the discharge and can be roughly contemporaneous with the repolarization of the myocardial cells or shorter. Thus, the recharge of the output capacitor may itself be additive or subtractive of the repolarization waveform. This may result in the further complication of the ability of the sense amplifier to respond shortly after the stimulus is delivered. To offset this problem, various circuits have been devised to provide a fast recharge of the output capacitor, such as the commonly assigned copending U.S. patent application Ser. No. 184,777, filed Sept. 8, 1980, entitled Body Stimulator, and Ser. No. 252,538, filed Apr. 9, 1981 entitled FAST RECHARGE OUTPUT CIRCUIT, now U.S. Pat. No. 4,406,286. The method and apparatus of the present invention is envisaged to operate in conjunction with such Fast Recharge Output Circuits.
In addition, and as a further complication to the design of pacemaker sense amplifier circuits, it may become necessary in atrial and ventricular synchronous pacemaker design to provide a blanking, that is a disconnecting of the input terminals of one or more of the sense amplifiers from the respective lead electrodes, following the delivery of a stimulting pulse on the same or other set of output terminals. For example, in an unipolar atrial synchronous pacemaker, it is necessary to blank the ventricular sense amplifier during the delivery of the stimulus by the atrial output circuit, since the atrial output signal is strong enough, after passing through the heart muscle, to be detected by the ventricular sense amplifier which would register a false sensing of an R wave. It is desirable that the ventricular sense amplifier be blanked for a very short interval so that it may be made ready to sense the ventricular depolarization, if any, triggered by the atrial stimulus after the A-V interval, or any premature ventricular contraction. The sensing of the ventricular depolarization would obviate the necessity of the pulse generator from providing a synchronized ventricular stimulation following the atrial stimulation.
The present invention overcomes the problem arising from polarization voltages present on a lead. In certain cases, the polarization voltage may cause the ventricular sense amplifier to register a false sense signal at the end of the ventricular blanking period, since the reconnection of the ventricular sense amplifier input terminals may itself cause some voltage transients, which, when coupled to a higher slew rate repolarization voltage, be sufficient to trigger the ventricular sense amplifier.
In other cases, the repolarization signals or T wave superimposed on the polarization voltage could have a high enough slew rate to trigger the sense amplifier, causing inappropriate T wave sensing. This can occur with interference signals.